Photobiomodulation for Hashimoto Thyroiditis

Hashimoto thyroiditis often begins long before someone becomes overtly hypothyroid.

For years, the thyroid may still produce enough hormone to keep TSH, FT4 and FT3 within range, while autoimmune activity continues quietly in the background. TPO or thyroglobulin antibodies may be very high, inflammation persists, oxidative stress increases, and functioning thyroid tissue is gradually lost.

That is the stage that interests me most.

If there is still viable thyroid tissue, the question is not only how to replace lost hormone later. It is whether we can do anything now to support the gland that remains.

Photobiomodulation, or PBM, is one possible tool.

PBM uses specific wavelengths of red and near-infrared light to influence mitochondrial function, oxidative stress and inflammatory signalling. Early human studies in Hashimoto thyroiditis suggest that carefully dosed treatment over the thyroid may improve some of these processes and, in selected patients, may even reduce thyroid hormone requirements.

It is not a replacement for thyroid medication or medical assessment. It is an adjunct aimed at supporting the thyroid itself.

Hashimoto is not simply a disease of “low thyroid hormone”.

By the time hypothyroidism is obvious on blood tests, the autoimmune process may have been active for many years.

During that time, thyroid tissue may be exposed to:

• ongoing immune attack
• local inflammation
• oxidative stress
• mitochondrial dysfunction
• gradual loss of functioning thyroid cells

Some people remain biochemically euthyroid despite very high antibody levels.

That matters because there may still be a window in which we are not simply replacing what has already been lost. We may also be able to support the thyroid tissue that is still functioning.

The thyroid is unusually vulnerable to oxidative stress.

It actually uses hydrogen peroxide as part of normal thyroid hormone production, which means it already operates in a biologically demanding environment. Add autoimmune inflammation to that, and the burden on thyroid cells increases further.

PBM is interesting because it acts at several points that matter here:

• mitochondrial function
• cellular energy production
• oxidative signalling
• nitric oxide pathways
• local inflammation
• tissue recovery

The aim is not to “blast the thyroid with red light”.

The aim is to use a measured dose of light to make the environment around surviving thyroid cells less hostile.

This is no longer just laboratory theory.

Human studies of thyroid-directed PBM have reported:

• reductions in TPO antibodies in some patients
• reductions in thyroglobulin antibodies in some studies
• improvements in thyroid ultrasound appearance
• improvements in oxidative stress markers
• improvements in quality of life
• changes in thyroid hormone indices
• lower levothyroxine requirements in some patients

In a randomized placebo-controlled trial using 830 nm low-level laser therapy, the treated group required significantly less levothyroxine at nine months, had lower TPO antibody levels, and showed improved thyroid ultrasound echogenicity. Thyroglobulin antibodies did not significantly differ between groups.

Longer-term follow-up suggested that some of that functional benefit persisted.

That does not mean PBM reverses Hashimoto or works for everyone.

It does mean there is enough human evidence to take the therapy seriously.

The patients who interest me most are not necessarily those with the most advanced hypothyroidism.

They are often people with:

• very high TPO antibodies
• very high thyroglobulin antibodies
• clear autoimmune thyroid disease
• thyroid function that is still normal or only mildly impaired
• evidence that there is still functioning thyroid tissue to protect

That is where the biological argument for PBM is strongest.

Once a thyroid has been extensively destroyed, there is obviously less tissue left to support.

With PBM, the aim is not to deliver as much light as possible. The aim is to deliver the right amount.

The SOHL Compact is a relatively powerful panel at 15 cm. Three minutes already delivers a substantial treatment dose to the front of the neck, and extending the session does not automatically make the treatment more effective.

PBM has what is called a biphasic dose response. In simple terms, there is a therapeutic window.

• Too little may do very little.
• The right dose may trigger a useful biological response.
• Push the dose much higher and you may simply gain no additional benefit.
  

  That is why the treatment time is deliberately short.

  Three minutes is not a token exposure. With this panel, at this distance, it is already a meaningful PBM dose.

I do not regard PBM as something patients should simply try and then judge by feel.

If we are going to use it, I want to know whether it is actually doing anything.

Before starting, I usually document:

• TSH
• Free T4
• Free T3
• TPO antibodies
• thyroglobulin antibodies
• current thyroid medication dose

Depending on the individual, I may also look at:

• vitamin D
• ferritin and iron studies
• selenium
• iodine status
• inflammatory markers

I usually repeat thyroid function after around 6–8 weeks and thyroid antibodies after approximately 12 weeks.

The goal is not to chase one antibody result from week to week. What matters is the trend.

Continue prescribed thyroid medication unless advised otherwise.
PBM is not a reason to stop levothyroxine.
However, one of the more interesting findings in the published studies has been that some patients required less levothyroxine after treatment.
That means monitoring matters.
If the thyroid begins producing more hormone while the same medication dose continues, a patient may become over-replaced.
Symptoms such as palpitations, tremor, heat intolerance, increased resting heart rate, sweating, marked insomnia or unexplained weight loss should prompt review.

I would not start thyroid PBM without further assessment in someone with:

• an unexplained thyroid nodule
• suspected or known thyroid malignancy
• a rapidly enlarging thyroid or neck mass
• unexplained cervical lymphadenopathy
• active untreated hyperthyroidism
• active Graves disease

A previously assessed benign thyroid nodule does not automatically rule PBM out, but it deserves individual consideration.

I would never look at a very high TPO antibody and assume the answer is simply three minutes in front of a red-light panel.

Hashimoto is an autoimmune disease, and the more important question is always:

Why is the immune system still being provoked?

That means looking at the wider picture.

Depending on the individual, I may assess:

• iron status
• vitamin D
• selenium
• iodine sufficiency
• metabolic health
• gut health
• sleep
• stress physiology
• medications
• environmental exposures
• other autoimmune conditions

The PBM is there to support the thyroid.

The rest of the work is about understanding the terrain in which the disease developed.

If you have Hashimoto thyroiditis, persistently high thyroid antibodies or ongoing thyroid symptoms, I can assess whether PBM has a reasonable role within a broader Functional Medicine plan.

Not a prettier antibody number.

Not a promise to “reverse” Hashimoto.

The aim is more practical:

reduce unnecessary inflammatory and oxidative stress, support the thyroid tissue that remains, preserve function where possible, and monitor whether the biology is moving in the right direction.

That is a much more useful goal.

Written by Dr Stephan Neff, MD, FANZCA, DipDHM — Functional & Integrative Medicine Doctor